Shigella induces epigenetic reprogramming of zebrafish neutrophils
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA896640 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22135214_1.fastq.gz | Fastqsanger.gz | |||
| SRR22135214_2.fastq.gz | Fastqsanger.gz | |||
| SRR22135215_1.fastq.gz | Fastqsanger.gz | |||
| SRR22135215_2.fastq.gz | Fastqsanger.gz | |||
| SRR22135216_1.fastq.gz | Fastqsanger.gz |
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Project description:Trained immunity is a long-term memory of innate immune cells, generating an improved response upon re-infection. Shigella is an important human pathogen and inflammatory paradigm for which there is no effective vaccine. Using zebrafish larvae we demonstrate that after Shigella priming neutrophils are more efficient at bacterial clearance. We observe that Shigella-induced protection is non-specific and long-lasting, and is unlike training by BCG and β-glucan. Analysis of histone ChIP-seq on primed neutrophils revealed that Shigella training deposits the active H3K4me3 mark on promoter regions of 1612 genes, significantly changing the epigenetic landscape of neutrophils towards enhanced microbial recognition and mitochondrial ROS production. Finally, we demonstrate that mitochondrial ROS plays a key role in enhanced antimicrobial activity of trained neutrophils. It is envisioned that signals and mechanisms we discover here can be used in other vertebrates, including humans, to suggest new therapeutic strategies involving neutrophils to control bacterial infection.
2023-09-13 | GSE217063 | GEO
Project description:Trained immunity is a long-term memory of innate immune cells, generating an improved response upon reinfection. Shigella is an important human pathogen and inflammatory paradigm for which there is no effective vaccine. Using zebrafish larvae, we demonstrate that after Shigella training, neutrophils are more efficient at bacterial clearance. We observe that Shigella-induced protection is nonspecific and has differences with training by BCG and β-glucan. Analysis of histone ChIP-seq on trained neutrophils revealed that Shigella training deposits the active H3K4me3 mark on promoter regions of 1612 genes, dramatically changing the epigenetic landscape of neutrophils toward enhanced microbial recognition and mitochondrial ROS production. Last, we demonstrate that mitochondrial ROS plays a key role in enhanced antimicrobial activity of trained neutrophils. It is envisioned that signals and mechanisms we discover here can be used in other vertebrates, including humans, to suggest new therapeutic strategies involving neutrophils to control bacterial infection.
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Project description:Shigella flexneri is historically regarded as the primary agent of bacillary dysentery, yet the closely-related Shigella sonnei is replacing S. flexneri, especially in developing countries. The underlying reasons for this dramatic shift are mostly unknown. Using a zebrafish (Danio rerio) model of Shigella infection, we discover that S. sonnei is more virulent than S. flexneri in vivo. Whole animal dual-RNAseq and testing of bacterial mutants suggest that S. sonnei virulence depends on its O-antigen oligosaccharide (which is unique among Shigella species). We show in vivo using zebrafish and ex vivo using human neutrophils that S. sonnei O-antigen can mediate neutrophil tolerance. Consistent with this, we demonstrate that O-antigen enables S. sonnei to resist phagolysosome acidification and promotes neutrophil cell death. Chemical inhibition or promotion of phagolysosome maturation respectively decreases and increases neutrophil control of S. sonnei and zebrafish survival. Strikingly, larvae primed with a sublethal dose of S. sonnei are protected against a secondary lethal dose of S. sonnei in an O-antigen-dependent manner, indicating that exposure to O-antigen can train the innate immune system against S. sonnei. Collectively, these findings reveal O-antigen as an important therapeutic target against bacillary dysentery, and may explain the rapidly increasing S. sonnei burden in developing countries.
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Project description:Background Compelling evidence indicates that Shigella species, the etiologic agents of bacillary dysentery, as well as enteroinvasive Escherichia coli, are derived from multiple origins of Escherichia coli and form a single pathovar. To further understand the genome diversity and virulence evolution of Shigella, comparative genomic hybridization microarray analysis was employed to compare the gene content of E. coli K-12 with those of 43 Shigella strains from all serotypes. Results For the 43 strains subjected to CGH microarray analyses, the common backbone of the Shigella genome was estimated to contain more than 1,900 open reading frames, with a mean number of 729 undetectable ORFs. The mosaic distribution of absent regions indicated that insertions and/or deletions have led to the highly diversified genomes of pathogenic strains. Conclusion These results support the hypothesis that by gain and loss of functions, Shigella species became successful human pathogens through convergent evolution from diverse genomic backgrounds. Moreover, we also found many specific differences between different lineages, providing a window into understanding bacterial speciation and taxonomic relationships. Keywords: comparative genomic hybridization
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Project description:Inflammasome regulates the host response to intracellular pathogens including mycobacteria. We have previously shown that the course of M. marinum infection in adult zebrafish (Danio rerio) has similar features than the course of tuberculosis in human. Here we have investigated the role of the inflammasome adaptor pycard in M. marinum infection in zebrafish with two CRISPR/Cas9 mutagenesis generated zebrafish line. Adult zebrafish devoid of pycard showed impaired survival and increased bacterial burden in M. marinum infection. Transcriptome analysis with RNA sequencing of a kidney derived neutrophils of M. marinum infected fish homozygous for pycardptu4 mutation revealed differentially expressed genes compared to WT controls. Differentially expressed genes were associated with neutrophil degranulation, haematopoiesis and PI3K signalling are differentially expressed in the pycard deficient neutrophils when compared to wild type controls.
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